Catalog No.S3032 Synonyms: AF 2838

Bindarit  Chemical Structure

Molecular Weight(MW): 324.37

Bindarit exhibits selective inhibition against monocyte chemotactic proteins MCP-1/CCL2, MCP-3/CCL7 and MCP-2/CCL8.

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In DMSO USD 220 In stock
USD 170 In stock
USD 470 In stock
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2 Customer Reviews

  • Differential participation of ATRs or MCP-1/CCR2 signaling in RVLM in pressor response and tachycardia after stroke. Changes in mean diastolic (ΔDBP) blood pressure or heart rate (ΔHR) relative to baseline in rats that received pretreatment by microinjection bilaterally into the RVLM of bindarit (Bin; 10 nmol, MCP-1 synthesis inhibitor), BMS CCR2 22 (BMS; 10 pmol, CCR2 antagonist), propagermanium (Prop; 10 pmol, CCR2 antagonist) or vehicle control (Veh).Values are mean ± SEM, n = 5-7 animals per experimental group. *P < 0.05 versus SC group, and +P < 0.05 versus Veh (Saline) + MCAO group in the post hoc Scheffe multiple-range test.

    Neurobiol Dis 2014 71, 292-304. Bindarit purchased from Selleck.

    Bindarit reduced the apoptosis in AngII induced hPMVECs. hPMVECs, human pulmonary microvascular endothelial cells; AngII, angiotensin II; PI, Propidium Iodide. FITC, fluoresceine isothiocyanate. Bnd, bindarit.

    Am J Transl Res, 2016, 8(1):28-36.. Bindarit purchased from Selleck.

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Choose Selective Immunology & Inflammation related Inhibitors

Biological Activity

Description Bindarit exhibits selective inhibition against monocyte chemotactic proteins MCP-1/CCL2, MCP-3/CCL7 and MCP-2/CCL8.
Features Bindarit is devoid of immunosuppressive effects.
MCP-1/CCL2 [1] MCP-3/CCL7 [1] MCP-2/CCL8 [1]
In vitro

Bindarit treatment causes a dose-dependent inhibition of the capacity of human monocytes to produce monocyte chemotactic protein-1 (MCP-1) in response to bacterial LPS or C. albicans with IC50 of 172 µM and 403 µM, respectively. The inhibition of LP-induced MCP-1 production by Bindarit is associated with reduced levels of MCP-1 mRNA transcripts with IC50 of 75 µM. Bindarit inhibits the production of MCP-1 by LPS-stimulated MM6 cells with IC50 of 425 μM, without affecting the release of IL-8 or IL-6. [2] Bindarit treatment inhibits the release of MCP-1 from IL-1 stimulated osteoblast cell line Saos-2. [3] Bindarit, even at the maximal concentration, does not exhibit a direct in vitro cytotoxic effect on human IIB-MEL-J melanoma or ECs, although it inhibits MCP-1 expression. [4] Bindarit (10-300 μM) reduces rat vascular smooth muscle cell (VSMC) proliferation, migration, and invasion. [5] Bindarit induces the downregulation of the classical NF-κB pathway. Bindarit displays a specific inhibitory effect on the p65 and p65/p50 induced MCP-1 promoter activation, with no effect on other tested activated promoters, indicating that Bindarit acts on a specific subpopulation of NF-κB isoforms and selects its targets within the whole NF-κB inflammatory pathway. [6] Bindarit modulates cancer-cell proliferation and migration, mainly through negative regulation of TGF-β and AKT signaling. [7]

In vivo Oral administration of Bindarit at 50 mg/kg in NZB/W mice delays the onset of proteinuria, significantly protects from renal function impairment, and prolongs survival of NZB/W mice or lupus mice. Bindarit treatment completely MCP-1 up-regulation during the progression of nephritis. [1] Inhibition of MCP-1 with Bindarit also reduces tumor growth and macrophage recruitment, rendering necrotic tumor masses in human melanoma xenografts. [4] Bindarit is effective in reducing neointima formation in both non-hyperlipidaemic and hyperlipidaemic animal models of vascular injury by a direct effect on VSMC proliferation and migration and by reducing neointimal macrophage content. [5] Administration of Bindarit results in impaired metastatic disease in prostate cancer PC-3M-Luc2 xenograft mice and impairment of local tumorigenesis in Balb/c mice with murine breast cancer 4T1-Luc cells. In addition, Bindarit treatment significantly decreases the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in 4T1-Luc primary tumors. [7]


Animal Research:


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  • Animal Models: NZB/W F1 female mice with a spontaneous autoimmune disease
  • Formulation: Formulated in 0.5% carboxy-methylcellulose
  • Dosages: ~50 mg/kg/day
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 64 mg/mL (197.3 mM)
Ethanol 64 mg/mL (197.3 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order:
0.5% CMC
For best results, use promptly after mixing.
7 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 324.37


CAS No. 130641-38-2
Storage powder
Synonyms AF 2838

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01269242 Completed Coronary Restenosis Aziende Chimiche Riunite Angelini Francesco S.p.A January 2009 Phase 2
NCT01109212 Completed Diabetic Nephropathy Aziende Chimiche Riunite Angelini Francesco S.p.A|Mario Negri Institute for Pharmacological Research March 2007 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID